Extubating trauma patients in the emergency department.

BACKGROUND: Trauma patients often require endotracheal intubation for urgent or emergent airway protection or to allow expeditious imaging when they cannot cooperate with the needed evaluation. These patients may occasionally be extubated in the emergency department (ED) when the trauma workup is negative for consequential injuries and eventually discharged from the ED. The timing and safety of discharging these patients is unclear. OBJECTIVE: The objective of this study was to identify the adverse outcomes and evaluate the safety of extubating trauma patients who are clinically well following evaluation in the ED. METHODS: Records of trauma patients who were intubated and then extubated in the ED at a single level 1 trauma referral center during the 4-year study period (Jan 2014 - Dec 2017) were retrospectively abstracted. The primary outcome was the incidence of a post-extubation complication, including desaturation, emesis, aspiration, need for sedative administration, or unplanned reintubation. Additional outcome measures included final disposition, duration of observation following extubation, ED length of stay and return to the hospital within 72 h. RESULTS: There were 59 eligible patients identified over the study period, of whom 95% presented following blunt trauma. One patient (1.7%; 95% confidence interval 0-9) required unplanned reintubation and developed aspiration pneumonia following re-extubation. Forty-two (71%) of the patients were discharged from the ED following extubation and a period of post-extubation observation with a mean of 5.8 h (0.6-16.7 h). None of the patients who were discharged returned to the ED within 72 h with complications related to extubation (0%; 95% confidence interval 0-6%). CONCLUSIONS: Patients presenting to the ED with possible acute traumatic injuries who are intubated and then extubated after trauma evaluation and resolution of the indication for intubation appear to have a low incidence of complication or return visit when discharged from the ED after a brief period of observation. Specific extubation and discharge criteria should be developed to ensure the safety of this practice. Further validation is required in the form of larger and prospective studies.

The effects of airway pressure release ventilation on respiratory mechanics in extrapulmonary lung injury.

BACKGROUND: Lung injury is often studied without consideration for pathologic changes in the chest wall. In order to reduce the incidence of lung injury using preemptive mechanical ventilation, it is important to recognize the influence of altered chest wall mechanics on disease pathogenesis. In this study, we hypothesize that airway pressure release ventilation (APRV) may be able to reduce the chest wall elastance associated with an extrapulmonary lung injury model as compared with low tidal volume (LVt) ventilation. METHODS: Female Yorkshire pigs were anesthetized and instrumented. Fecal peritonitis was established, and the superior mesenteric artery was clamped for 30 min to induce an ischemia/reperfusion injury. Immediately following injury, pigs were randomized into (1) LVt (n = 3), positive end-expiratory pressure (PEEP) 5 cmH2O, V t 6 cc kg(-1), FiO2 21 %, and guided by the ARDSnet protocol or (2) APRV (n = 3), P High 16-22 cmH2O, P Low 0 cmH2O, T High 4.5 s, T Low set to terminate the peak expiratory flow at 75 %, and FiO2 21 %. Pigs were monitored continuously for 48 h. Lung samples and bronchoalveolar lavage fluid were collected at necropsy. RESULTS: LVt resulted in mild acute respiratory distress syndrome (ARDS) (PaO2/FiO2 = 226.2 ± 17.1 mmHg) whereas APRV prevented ARDS (PaO2/FiO2 = 465.7 ± 66.5 mmHg; p < 0.05). LVt had a reduced surfactant protein A concentration and increased histologic injury as compared with APRV. The plateau pressure in APRV (34.3 ± 0.9 cmH2O) was significantly greater than LVt (22.2 ± 2.0 cmH2O; p < 0.05) yet transpulmonary pressure between groups was similar (p > 0.05). This was because the pleural pressure was significantly lower in LVt (7.6 ± 0.5 cmH2O) as compared with APRV (17.4 ± 3.5 cmH2O; p < 0.05). Finally, the elastance of the lung, chest wall, and respiratory system were all significantly greater in LVt as compared with APRV (all p < 0.05). CONCLUSIONS: APRV preserved surfactant and lung architecture and maintenance of oxygenation. Despite the greater plateau pressure and tidal volumes in the APRV group, the transpulmonary pressure was similar to that of LVt. Thus, the majority of the plateau pressure in the APRV group was distributed as pleural pressure in this extrapulmonary lung injury model. APRV maintained a normal lung elastance and an open, homogeneously ventilated lung without increasing lung stress.